Efficient replication of severe acute respiratory syndrome coronavirus in mouse cells is limited by murine angiotensin-converting enzyme 2
dc.contributor.author | Li, Wenhui | |
dc.contributor.author | Greenough, Thomas C. | |
dc.contributor.author | Moore, Michael J. | |
dc.contributor.author | Vasilieva, Natalya | |
dc.contributor.author | Somasundaran, Mohan | |
dc.contributor.author | Sullivan, John L. | |
dc.contributor.author | Farzan, Michael | |
dc.contributor.author | Choe, Hyeryun | |
dc.date | 2022-08-11T08:10:12.000 | |
dc.date.accessioned | 2022-08-23T16:58:52Z | |
dc.date.available | 2022-08-23T16:58:52Z | |
dc.date.issued | 2004-10-01 | |
dc.date.submitted | 2012-05-01 | |
dc.identifier.citation | J Virol. 2004 Oct;78(20):11429-33. <a href="http://dx.doi.org/10.1128/JVI.78.20.11429-11433.2004">Link to article on publisher's site</a> | |
dc.identifier.issn | 0022-538X (Linking) | |
dc.identifier.doi | 10.1128/JVI.78.20.11429-11433.2004 | |
dc.identifier.pmid | 15452268 | |
dc.identifier.uri | http://hdl.handle.net/20.500.14038/43459 | |
dc.description.abstract | Replication of viruses in species other than their natural hosts is frequently limited by entry and postentry barriers. The coronavirus that causes severe acute respiratory syndrome (SARS-CoV) utilizes the receptor angiotensin-converting enzyme 2 (ACE2) to infect cells. Here we compare human, mouse, and rat ACE2 molecules for their ability to serve as receptors for SARS-CoV. We found that, compared to human ACE2, murine ACE2 less efficiently bound the S1 domain of SARS-CoV and supported less-efficient S protein-mediated infection. Rat ACE2 was even less efficient, at near background levels for both activities. Murine 3T3 cells expressing human ACE2 supported SARS-CoV replication, whereas replication was less than 10% as efficient in the same cells expressing murine ACE2. These data imply that a mouse transgenically expressing human ACE2 may be a useful animal model of SARS. | |
dc.language.iso | en_US | |
dc.relation | <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=15452268&dopt=Abstract">Link to Article in PubMed</a> | |
dc.relation.url | http://www.ncbi.nlm.nih.gov/pmc/articles/PMC521845/pdf/0880-04.pdf | |
dc.subject | 3T3 Cells | |
dc.subject | Animals | |
dc.subject | Cell Line | |
dc.subject | Endopeptidases | |
dc.subject | Humans | |
dc.subject | Mice | |
dc.subject | Peptidyl-Dipeptidase A | |
dc.subject | Rats | |
dc.subject | SARS Virus | |
dc.subject | Severe Acute Respiratory Syndrome | |
dc.subject | *Virus Replication | |
dc.subject | Immunology and Infectious Disease | |
dc.subject | Pediatrics | |
dc.title | Efficient replication of severe acute respiratory syndrome coronavirus in mouse cells is limited by murine angiotensin-converting enzyme 2 | |
dc.type | Journal Article | |
dc.source.journaltitle | Journal of virology | |
dc.source.volume | 78 | |
dc.source.issue | 20 | |
dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/peds_immunology/41 | |
dc.identifier.contextkey | 2814371 | |
html.description.abstract | <p>Replication of viruses in species other than their natural hosts is frequently limited by entry and postentry barriers. The coronavirus that causes severe acute respiratory syndrome (SARS-CoV) utilizes the receptor angiotensin-converting enzyme 2 (ACE2) to infect cells. Here we compare human, mouse, and rat ACE2 molecules for their ability to serve as receptors for SARS-CoV. We found that, compared to human ACE2, murine ACE2 less efficiently bound the S1 domain of SARS-CoV and supported less-efficient S protein-mediated infection. Rat ACE2 was even less efficient, at near background levels for both activities. Murine 3T3 cells expressing human ACE2 supported SARS-CoV replication, whereas replication was less than 10% as efficient in the same cells expressing murine ACE2. These data imply that a mouse transgenically expressing human ACE2 may be a useful animal model of SARS.</p> | |
dc.identifier.submissionpath | peds_immunology/41 | |
dc.contributor.department | Program in Molecular Medicine | |
dc.contributor.department | Department of Pediatrics | |
dc.source.pages | 11429-33 |